VX-11eERK inhibitor CAS# 896720-20-0 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 896720-20-0 | SDF | Download SDF |
| PubChem ID | 11634725 | Appearance | Powder |
| Formula | C24H20Cl2FN5O2 | M.Wt | 500.35 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | VX 11e | ||
| Solubility | DMSO : ≥ 100 mg/mL (199.86 mM) H2O : < 0.1 mg/mL (insoluble) *"≥" means soluble, but saturation unknown. | ||
| Chemical Name | 4-[2-(2-chloro-4-fluoroanilino)-5-methylpyrimidin-4-yl]-N-[(1S)-1-(3-chlorophenyl)-2-hydroxyethyl]-1H-pyrrole-2-carboxamide | ||
| SMILES | CC1=CN=C(N=C1C2=CNC(=C2)C(=O)NC(CO)C3=CC(=CC=C3)Cl)NC4=C(C=C(C=C4)F)Cl | ||
| Standard InChIKey | WUTVMXLIGHTZJC-OAQYLSRUSA-N | ||
| Standard InChI | InChI=1S/C24H20Cl2FN5O2/c1-13-10-29-24(31-19-6-5-17(27)9-18(19)26)32-22(13)15-8-20(28-11-15)23(34)30-21(12-33)14-3-2-4-16(25)7-14/h2-11,21,28,33H,12H2,1H3,(H,30,34)(H,29,31,32)/t21-/m1/s1 | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Potent and selective extracellular signal-related kinase 2 (ERK2) inhibitor (Ki values are <2, 395, 540 and 852 nM for ERK2, GSK-3, Aurora Kinase A and Cdk2 respectively). Potently blocks proliferation of HT29 cells (IC50 = 48 nM). Orally bioavailable. |
VX-11e Dilution Calculator
VX-11e Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 1.9986 mL | 9.993 mL | 19.986 mL | 39.972 mL | 49.965 mL |
| 5 mM | 0.3997 mL | 1.9986 mL | 3.9972 mL | 7.9944 mL | 9.993 mL |
| 10 mM | 0.1999 mL | 0.9993 mL | 1.9986 mL | 3.9972 mL | 4.9965 mL |
| 50 mM | 0.04 mL | 0.1999 mL | 0.3997 mL | 0.7994 mL | 0.9993 mL |
| 100 mM | 0.02 mL | 0.0999 mL | 0.1999 mL | 0.3997 mL | 0.4997 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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VX-11e is a potent and selective inhibitor of ERK [1].
ERK is extracellular signal-regulated kinases. The Ras/Raf/MEK/ERK signal transduction is an oncogenic pathway related to a variety of human cancers [1].
References:
[1]. Aronov, Alex M, Tang Q, et al. Martinez-Botella, Gabriel et al. Structure-Guided Design of Potent and Selective Pyrimidylpyrrole Inhibitors of Extracellular Signal-Regulated Kinase (ERK) Using Conformational Control. Journal of Medicinal Chemistry, 2009, 52(20): 6362-6368.
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Involvement of FAK-ERK2 signaling pathway in CKAP2-induced proliferation and motility in cervical carcinoma cell lines.[Pubmed:28522860]
Sci Rep. 2017 May 18;7(1):2117.
Cervical carcinoma is the fourth most common cause of death in woman, caused by human papillomavirus (HPV) infections and arising from the cervix. Cytoskeleton-associated protein 2 (CKAP2), also known as tumor-associated microtubule-associated protein, has been linked to tumorigenic effects. In the present study, we screened CKAP2 as a new candidate gene which promotes development of cervical carcinoma, in two independent datasets (TCGA and GSE27678). Results showed that CKAP2 expression was significantly up-regulated in cervical cancerous tissues compared with normal counterparts. Gene set enrichment analysis (GSEA) showed that metastasis, cell cycle and FAK pathways were related with elevated CKAP2 expression. Knockdown of CKAP2 expression significantly inhibited cell proliferation, migration and invasion both in HeLa and C-33A cells. And depletion of CKAP2 down-regulated the expression of metastasis and cell cycle related proteins as well as the phosphorylation of ERK2 (p-ERK2), except E-cadherin. In vivo experiment revealed that knockdown of CKAP2 inhibited C-33A cells proliferation. However, FAK inhibitor PF-562271 and ERK2 inhibitor VX-11e treatment significantly inhibited CKAP2 overexpression-induced cell proliferation, migration and invasion in SiHa cells. In conclusion, our study suggests that CKAP2 acts as a functional oncogene in cervical carcinoma development and may exert its function by targeting FAK-ERK2 signaling pathway.
Personalized Preclinical Trials in BRAF Inhibitor-Resistant Patient-Derived Xenograft Models Identify Second-Line Combination Therapies.[Pubmed:26673799]
Clin Cancer Res. 2016 Apr 1;22(7):1592-602.
PURPOSE: To test second-line personalized medicine combination therapies, based on genomic and proteomic data, in patient-derived xenograft (PDX) models. EXPERIMENTAL DESIGN: We established 12 PDXs from BRAF inhibitor-progressed melanoma patients. Following expansion, PDXs were analyzed using targeted sequencing and reverse-phase protein arrays. By using multi-arm preclinical trial designs, we identified efficacious precision medicine approaches. RESULTS: We identified alterations previously described as drivers of resistance: NRAS mutations in 3 PDXs, MAP2K1 (MEK1) mutations in 2, BRAF amplification in 4, and aberrant PTEN in 7. At the protein level, re-activation of phospho-MAPK predominated, with parallel activation of PI3K in a subset. Second-line efficacy of the pan-PI3K inhibitor BKM120 with either BRAF (encorafenib)/MEK (binimetinib) inhibitor combination or the ERK inhibitor VX-11e was confirmed in vivo Amplification of MET was observed in 3 PDX models, a higher frequency than expected and a possible novel mechanism of resistance. Importantly, MET amplification alone did not predict sensitivity to the MET inhibitor capmatinib. In contrast, capmatinib as single agent resulted in significant but transient tumor regression in a PDX with resistance to BRAF/MEK combination therapy and high pMET. The triple combination capmatinib/encorafenib/binimetinib resulted in complete and sustained tumor regression in all animals. CONCLUSIONS: Genomic and proteomic data integration identifies dual-core pathway inhibition as well as MET as combinatorial targets. These studies provide evidence for biomarker development to appropriately select personalized therapies of patients and avoid treatment failures. See related commentary by Hartsough and Aplin, p. 1550.
Structure-guided design of potent and selective pyrimidylpyrrole inhibitors of extracellular signal-regulated kinase (ERK) using conformational control.[Pubmed:19827834]
J Med Chem. 2009 Oct 22;52(20):6362-8.
The Ras/Raf/MEK/ERK signal transduction, an oncogenic pathway implicated in a variety of human cancers, is a key target in anticancer drug design. A novel series of pyrimidylpyrrole ERK inhibitors has been identified. Discovery of a conformational change for lead compound 2, when bound to ERK2 relative to antitarget GSK3, enabled structure-guided selectivity optimization, which led to the discovery of 11e, a potent, selective, and orally bioavailable inhibitor of ERK.
